The Pentachlorophenol Metabolite Tetrachlorohydroquinone Induces Massive ROS and Prolonged p-ERK Expression in Splenocytes, Leading to Inhibition of Apoptosis and Necrotic Cell Death

doi:10.1371/journal.pone.0089483

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標題:	The Pentachlorophenol Metabolite Tetrachlorohydroquinone Induces Massive ROS and Prolonged p-ERK Expression in Splenocytes, Leading to Inhibition of Apoptosis and Necrotic Cell Death
作者:	Chen, Hsiu-Min Zhu, Ben-Zhan Chen, Rong-Jane Wang, Bour-Jr Wang, Ying-Jan
貢獻者:	化粧品應用與管理系
關鍵字:	OXIDATIVE DNA-DAMAGE N-ACETYLCYSTEINE MAP KINASES IN-VIVO HYDROGEN-PEROXIDE MAJOR METABOLITE PHOSPHATIDYLSERINE EXPOSURE MOLECULAR-MECHANISMS SIGNAL-TRANSDUCTION TUMOR PROMOTION
日期:	2014-02
上傳時間:	2015-05-06 21:26:12 (UTC+8)
出版者:	Public Library Science
摘要:	Pentachlorophenol (PCP) has been used extensively as a biocide and a wood preservative and has been reported to be immunosuppressive in rodents and humans. Tetrachlorohydroquinone (TCHQ) is a major metabolite of PCP. TCHQ has been identified as the main cause of PCP-induced genotoxicity due to reactive oxidant stress (ROS). However, the precise mechanisms associated with the immunotoxic effects of PCP and TCHQ remain unclear. The aim of this study was to examine the effects of PCP and TCHQ on the induction of ROS and injury to primary mouse splenocytes. Our results shown that TCHQ was more toxic than PCP and that a high dose of TCHQ led to necrotic cell death of the splenocytes through induction of massive and sudden ROS and prolonged ROS-triggered ERK activation. Inhibition of ROS production by N-acetyl-cysteine (NAC) partially restored the mitochondrial membrane potential, inhibited ERK activity, elevated caspase-3 activity and PARP cleavage, and, eventually, switched the TCHQ-induced necrosis to apoptosis. We suggest that prolonged ERK activation is essential for TCHQ-induced necrosis, and that ROS play a pivotal role in the different TCHQ-induced cell death mechanisms.
關聯:	Plos One, v.9 n.2, e89483
Appears in Collections:	[化妝品應用與管理系(所)] 期刊論文

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